Earn

4 CE credits
This course was written for dentists, dental hygienists, and assistants.

Dentinal Hypersensitivity: Etiology, Diagnosis and Management

A Peer-Reviewed Publication Written by Howard E. Strassler, DMD, FADM, FAGD, FACD and Francis G. Serio, DMD, MS, MBA, FICD, FACD, FADI

PennWell is an ADA CERP recognized provider ADA CERP is a service of the American Dental Association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, nor does it imply acceptance of credit hours by boards of dentistry. Concerns of complaints about a CE provider may be directed to the provider or to ADA CERP at www.ada.org/goto/cerp.

This course has been made possible through an unrestricted educational grant from Colgate-Palmolive Company. The cost of this CE course is $59.00 for 4 CE credits. Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

Educational Objectives
The overall goal of this course is to provide dental professionals with information on the etiology, diagnosis and treatment of dentinal hypersensitivity. Upon completion of this course, the participant will be able to do the following: 1. Know the incidence of dentinal hypersensitivity and risk factors for this condition 2. Know the anatomical and physiological features, and the accepted theory, associated with dentinal hypersensitivity 3. Understand the need for screening and diagnosis by exclusion for dentinal hypersensitivity 4. Know the treatment options available for dentinal hypersensitivity and considerations in selecting these.

Abstract
Dentinal hypersensitivity has been referred to as one of the most painful and chronic dental conditions, with a reported prevalence of between 4% and 57% in the general population and a higher prevalence in periodontal patients. It may also occur as a result of, or during, dental treatment. Clinicians must screen for dentinal hypersensitivity and diagnose by exclusion, determine appropriate treatment, and provide treatment and preventive recommendations. Consideration should also be given to treating dentinal hypersensitivity associated with dental treatment. Traditional treatments have included adhesive resins, fluoride varnishes, HEMA, iontophoresis, gingival grafts and desensitizing dentifrices. Other technologies include the use of bioglass particles, ACP, as well as 8% arginine and calcium carbonate paste.

Introduction
During routine dental examinations, our patients frequently inquire about dentinal hypersensitivity that was one episode or is chronic and recurring due to a given action, e.g., drinking cold beverages, eating hot foods, breathing in and out. This common complaint is defined as dentinal hypersensitivity, but it is also known as root sensitivity, or just sensitivity. Patients describe this phenomenon as sharp, short-lasting tooth pain, irrespective of the stimulus.1 Holland et al. described dentinal hypersensitivity as characterized by short, sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other form of dental defect or pathology.2 The prevalence of dentinal hypersensitivity has been reported to be between 4% and 57% in the general population.3-10 Among periodontal patients, its frequency is considerably higher (60%98%).11,12 This hypersensitivity may be due to cementum removal during root instrumentation. Dentinal hypersensitivity has been described as generally occurring in patients 30 to 40 years old,13 but it can occur in patients significantly younger or older. Women may be affected more often than men.14 Dentinal hypersensitivity af2

fects incisors, canines, premolars and molars, with canines and premolars reported to be affected most often.15,16 Patients with dentinal hypersensitivity may not specifically seek treatment, because they do not view it as a significant dental health problem, but will mention it at a routine dental appointment.17 At other times, patients will seek treatment recommendations from their dental professionals. Some patients are concerned whenever there is dental pain,18 and for some the first time they experience dentinal hypersensitivity creates fear that there is something more serious occurring. The authors of this course have had patients report sensitivity who believe that it may be a toothache that requires immediate attention so that the pain does not get worse. Patients can identify areas of dentinal hypersensitivity before a clinical exam is performed. This may be chronic, or unpredictable and cause intermittent discomfort that is difficult to pinpoint.19,20 Other patients cannot distinguish between dentinal sensitivity and gingival sensitivity. Patients may also experience dentinal hypersensitivity as a result of treatment such as scaling and root planing or during routine and normal actions associated with treatment, such as when a tooth is dried using an air spray or scratched with the tip of an explorer. Dental treatment can also exacerbate pre-existing sensitivity. Dentinal hypersensitivity has all the criteria to be considered a true pain syndrome.21 It is important to distinguish sensitivity pain, that of short duration, from pain of longer duration not treatable with desensitizing agents. A painful response that lingers or that wakens the person from a sound sleep may be the result of pulpal inflammation. A diagnosis by the dentist is necessary to establish a cause and effect, and a diagnosis by exclusion must be made for dentinal hypersensitivity, ruling out other conditions requiring different treatment. After the diagnosis of dentinal hypersensitivity has been made, depending on the etiology, recommendations can be made for effective treatment. Calvo noted in 1884: There is great need of a medicament, which while lessening the sensitivity of dentin, will not impair the vitality of the pulp.22 Recommendations can include in-office, at-home professionally dispensed or over-the counter treatments.23-26 Regardless of which treatment recommendations are made and provided, it is important to follow up with the patient to evaluate the therapeutic results.

Etiology and Physiology of Dentinal Hypersensitivity

Dentinal hypersensitivity can have multiple etiologies. It is important that the patients medical and social history, lifestyle, medications and supplements being taken, diet and food habits, and oral hygiene be thoroughly reviewed. Before making a diagnosis of dentinal hypersensitivity, other oral conditions must be ruled out, including occlusal trauma, caries, defective restorations, fractured or cracked
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teeth, potential reversible or irreversible pulpal pathology, or gingival conditions.14,24 For instance, pain during chewing may be due to a fractured and mobile restoration that is rubbing against the dentin or diagnostic for a cracked tooth.27 Dentin is sensitive due to its anatomy and physiology. It is a porous, mineralized connective tissue with an organic matrix of collagenous proteins and an inorganic component, hydroxyapatite. Dentinal tubules are micro-canals that radiate outward through the dentin from the pulp cavity to the dentinal surface, with different configurations and diameters in different teeth. For human dentin, one square millimeter can contain 30,000 tubules, depending on depth. Each tubule contains a Tomes fiber (cytoplastic cell process) and an odontoblast that communicates with the pulp. Within the dentinal tubules there are two types of nerve fibers, myelinated (A-fibers) and unmyelinated (C-fibers).28 The A-fibers are responsible for the sensation of dentinal hypersensitivity, perceived as pain in response to all stimuli. The most widely accepted mechanism of dentinal sensitivity is the hydrodynamic theory, first described by Brnnstrm.29,30 In this model, the aspiration of odontoblasts into the dentinal tubules, as an immediate effect of physical stimuli applied to exposed dentin, results in the outward flow of the tubular contents (dentinal fluids) through capillary action (Figure 1). The changes to the dentinal surface lead to stimulation of the A-type nerve fibers surrounding the odontoblasts. For there to be a stimulus response, the tubules must be open at both the dentinal interface and within the pulp. Absi and coworkers reported that nonsensitive teeth were not responsive to any physical stimuli; sensitive teeth had up to eight times the number of open dentinal tubules per surface area compared to nonresponsive teeth.31 Another theory is an alteration in pulpal sensory nerve activity.32 The treatment of exposed, open dentinal tubules is based upon the physiology of the stimulus response. Figure 1. The hydrodynamic theory

Location of Dentinal Hypersensitivity Patients at Risk

Why are some root surfaces hypersensitive and others are not? Exposed root surfaces due to gingival recession are a major predisposing factor to dentinal root hypersensitivity (Figure 2).33 According to a recent report of adults over the age of 60, almost 32% had root caries or a restored root surface.34 Since root caries are an indication of periodontal attachment loss and subsequent recession, this defines the population of adults over 60 with an at-risk of recession in at least one or more teeth as at least 30%. Another study concluded that at least 22% of the adult population between 30 and 90 years of age will have evidence of recession in one or more teeth of 3 mm or more.35 Gingival recession is more common as patients age and in patients with better oral hygiene.14,36 Common causes include inadequate attached gingiva, prominent roots with a thin alveolar housing or bony dehiscence, toothbrush abrasion, periodontal surgery, factitial habits (e.g., picking at cervical area of the tooth with a fingernail), excessive tooth cleaning, excessive flossing, loss of gingival attachment due to specific pathologies, and iatrogenic loss of attachment during restorative procedures.33,37 Figure 2. Gingival recession with exposed root surfaces Exposed lingual root surfaces

Dentinal hypersensitivity can also occur as a result of a routine dental cleaning, or be exacerbated during scaling and root planing or routine dental prophylaxis and polishing due to pre-existing dentin-root hypersensitivity. Patients who have had or are having periodontal therapy are at risk;12 the prevalence of root sensitivity has been reported as 9%23% before and 54%55% after periodontal therapy. An increase in the intensity of root sensitivity occurred one to three weeks following therapy, after which it slowly decreased. An assessment found that all patients experienced increased discomfort and dentinal hypersensitivity after periodontal treatment, including scaling and root planing.37 Fear of pain and discomfort during subgingival instrumentation has been reported to deter 10% of the population from seeking treatment.38 Once the root surfaces are exposed, the cementum/dentin is more susceptible to caries and loss of tooth substance due to erosion, abrasion and abfraction (Figure 3).39-42 Postprocedural
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sensitivity can also be a result of etching beyond restoration margins, leaving dentinal tubules open, or of finishing and polishing a restoration that extends to the root surfaces, which can also leave dentinal tubules open. Root surfaces on teeth adjacent to a tooth being extracted can be abraded and scarred with the use of dental elevators during the extraction procedure. Resective periodontal surgical procedures may also leave roots exposed. Enamel loss with exposed dentin due to attrition and tooth wear due to bruxism, occlusal habits and other forms of parafunctional activity can also contribute to the etiology of dentinal hypersensitivity (Figure 4).41 Figure 3. Gingival recession with associated noncarious cervical lesions

Biofilm deposits on root surfaces may also increase hypersensitivity. The opening of dentinal tubules can also occur due to poor oral hygiene techniques leaving bacterial plaque/ biofilm on root surfaces, with the acidic by-products of the biofilm opening the dentinal tubules. Conversely, overzealous oral hygiene techniques can cause continued dentinal tubule exposure. Root surfaces exposed to the physical action of toothbrushing with and without toothpaste can be predisposing factors in removing the smear layer, leaving a tooth hypersensitive.13,45 Exposure of the oral cavity to acids, e.g., ingestion of acidic foods and beverages46-48 or ingestion of chlorinated pool water,49 as well as bulimia and gastrointestinal reflux disease can also contribute to the opening of the end of the dentinal tubules (Figure 6).50 Brushing immediately after ingesting acidic foods or beverages should be avoided.51 Figure 6. Erosion of the maxillary anterior teeth in a bulemic patient due to stomach acid

Figure 4. Enamel loss with exposed dentin due to attrition

Screening and Diagnosis of Dentinal Hypersensitivity

Dentists and dental hygienists unfortunately do not all routinely include screening for dentinal hypersensitivity.25 In 1995, a random sample of Dutch dentists completed a survey on the prevalence, conditions and treatment of cervical hypersensitivity of their patients.52 A similar questionnaire was administered to U.K. dentists in 2002.53 For both groups, the results revealed discrepancies in screening, perceptions and knowledge of treatment. A separate study administered a questionnaire by mail to 5,000 dentists and 3,000 dental hygienists in Canada and revealed that fewer than half of the respondents considered a differential diagnosis for dentinal hypersensitivity, even though it is by definition a diagnosis of exclusion.25 Many misidentified the etiology: 64% of the dentists and 77% of the hygienists incorrectly cited bruxism and malocclusion as triggers for dentinal hypersensitivity, while only 7% of dentists and 5% of dental hygienists correctly identified erosion as a primary cause and 17% of dentists and 48% of hygienists were unable to identify the accepted theory of hypersensitivity. Only half of the respondents had the confidence to manage a patients pain and to consider the modification of predisposing factors to control a patients pain. This survey also demonstrated a lack of understanding of desensitizing toothpastes most dentists (56%) and dental hygienists (68%) believed these helped prevent dentinal
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In normal function, the tubules sclerose and become plugged, and when dentin is cut or abraded the mineralized matrix produces debris that spreads over the dentin surface to form a smear layer.43,44 This occurs to both enamel and dentin,44 but the loss of this smear layer, the unplugging of the dentinal tubules, contributes to dentinal hypersensitivity (Figure 5). Figure 5. Scanning electron micrograph demonstrating open dentinal tubules

hypersensitivity, while 31% and 16%, respectively, did not believe that desensitizing toothpastes provided relief from dentinal hypersensitivity. Dental professionals need to fully understand the etiology and treatment of dentinal hypersensitivity, to screen for it and to diagnose it by exclusion. It is also worth noting that patients with unresolved hypersensitivity over many years provide the dental professional with varied behavioral and postural clues, some of which are easily recognized. These include avoidance of routine dental exams, necessary treatment and follow-up care, reluctance to schedule planned treatment or follow-up care, insistence on the use of local anesthesia for even the most minor of dental treatments, tense facial muscles, tooth clenching, a rigid torso, holding hands tightly on the arm rest, crossed arms, an awkward head position and an inability to follow routine instructions for head and body positioning.19 As part of any screening for dentinal hypersensitivity, the clinician should assess whether there is a localized or generalized problem. In addition, for patients with identified isolated and generalized dentinal hypersensitivity, a routine dental cleaning can be anxiety provoking.38 Consideration should be given to dentinal hypersensitivity associated with dental treatment during treatment and postoperatively. While the focus of controlling pain for many dental professionals during periodontal scaling and root planing and routine dental cleanings has been the use of local and topical anesthetic agents,37,54,55 we should also give thought to providing our patients with treatments to relieve postprocedural dentinal hypersensitivity.19,26,56,57

be treated in-office. For generalized conditions where there is significant recession on multiple teeth, an at-home treatment regimen may be a better choice. Table 1. Preventive Recommendations for Dentinal Hypersensitivity Suggestions for patients: Avoid using large amounts of dentifrice or reapplying it during brushing. Avoid medium- or hard-bristle toothbrushes. Avoid brushing teeth immediately after ingesting acidic foods. Avoid overbrushing with excessive pressure or for an extended period of time. Avoid excessive flossing or improper use of other interproximal cleaning devices. Avoid picking or scratching at the gumline or using toothpicks inappropriately. Suggestions for professionals: Avoid overinstrumenting the root surfaces during scaling and root planing, particularly in the cervical area of the tooth. Avoid overpolishing exposed dentin during stain removal. Avoid violating the biologic width during restoration placement, as this may cause recession. Avoid burning the gingival tissues during in-office bleaching, and advise patients to be careful when using home bleaching products. Professional in-office treatments In-office desensitizing agents work by occluding and sealing the dentin tubules.62,63 When treating patients with an in-office treatment, American Dental Association treatment codes can be noted for insurance reimbursement (Table 2). Table 2. In-office desensitizing codes Miscellaneous services D9910 Application of desensitizing medicament Includes in-office treatment of root sensitivity. Typically reported on a per visit basis for application of topical fluoride or other desensitizing agents. This code is not used for bases, liners or adhesives used under restorations. D9911 Application of desensitizing resin for cervical and/or root surface Typically reported on a per tooth basis for application of adhesive resins. This code is not used for bases, liners or adhesives used under restorations. A recent novel approach is a technology based on arginine, a natural product, and calcium carbonate. This technology was introduced as a result of the need to provide patients with a treatment regimen to reduce and treat postprocedural dentinal hypersensitivity after dental cleanings. In 2002, Kleinberg et al. reported on the development of this novel desensitizing technology based upon the role that saliva plays in naturally reducing dentinal hypersensitivity. Saliva
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Treatment and Prevention of Dentinal Hypersensitivity

Once the diagnosis of dentinal hypersensitivity has been made and the etiologic factors identified, treatment and prevention should be primary goals,19,58,59 and a treatment plan can be developed and implemented. Once a tooth or teeth are predisposed to dentinal hypersensitivity, they will need to be re-evaluated for continued treatment. The patient should be shown correct brushing techniques to prevent further loss of dentin that would contribute to dentinal hypersensitivity; improper toothbrushing has also been associated with dentinal hypersensitivity.1 It has been shown that both a manual and a power brush used with a desensititizing toothpaste are almost equivalent in effectiveness.60 If there are changes and behavior modifications or treatments that can be made, these should be discussed with the patient. Drisko summarized preventive recommendations (Table 1).61

Treatment of Dentinal Hypersensitivity

Two major groups of products are used to treat dentinal hypersensitivity: those that block and occlude dentinal tubules, and those that interfere with the transmission of neural impulses. Localized dentinal hypersensitivity can usually
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provides calcium and phosphate, which over time will occlude and block open dentinal tubules from external stimuli associated with dentinal hypersensitivity.19,56 Reduced salivary flow, hyposalivation and xerostomia are risk factors for caries and tooth demineralization and may exacerbate dentinal hypersensitivity. While hyposalivation may be due to medical conditions and aging, it is also a side effect of more than 500 prescription and over-the-counter medications.64 The mechanism providing for the clinical effectiveness of this technology utilizes arginine, an amino acid; bicarbonate, a pH buffer; and calcium carbonate, a source of calcium. This technology, originally introduced as Sensistat (Ortek Therapeutics, Roslyn Heights, NY), effectively relieves dentinal hypersensitivity.56 The technology is proposed to block dentinal hypersensitivity pain by occluding dentinal tubules by using arginine, which is positively charged at physiologic pH of 6.5-7.5, to bind to the negatively charged dentin surface, and helps attract a calcium-rich layer from the saliva to infiltrate and block the dentinal tubules. An in-office product based upon this technology (ProClude) was used for the management of tooth sensitivity during professional dental cleanings. Early studies on this technology demonstrated instant relief from discomfort that lasted 28 days after a single application and reported a 71.7% reduction in sensitivity measured by air-blast and an 84.2% reduction by the scratch test immediately following application.56 The same technology was used in a toothpaste (DenClude). In 2007, Colgate-Palmolive Company acquired the rights to the technology, now known as Pro-Argin technology, and has introduced Colgate Sensitive Pro-Relief Desensitizing Paste (Figure 7). This is applied in-office using a prophylaxis cup on a prophy angle. The recommendation is that the paste be applied using a low speed handpiece with a moderate amount of pressure to burnish the paste into the exposed tubules, optimizing their occlusion. This product can be used before or after dental procedures. Figure 7. Colgate Sensitive Pro-Relief Desensitizing Paste

on these results, application of the paste pre-procedurally would reduce patient discomfort during scaling and root planing and thereby enable thorough treatment without causing patients pain. An evaluation of this desensitizing paste containing 8% arginine and calcium carbonate on dentin and enamel, as well as on restorative materials, found no significant effect on surface roughness.66 In investigating the mechanism of action of arginine and calcium carbonate paste using scanning electron microscopy, confocal laser scanning microscopy and atomic force microscopy, Petrou et al. found that the technology totally occluded the dentinal tubules rapidly. This was the result of the formation of a deposit on the surface and plugs in the dentinal tubules that contained high amounts of phosphate, calcium and carbonate. In addition, it was determined through hydraulic conductance testing that these deposits significantly reduced the flow of dentinal fluid in the tubules.67 Figure 8. Occlusion of dentinal tubules by the Pro-Argin technology

SEM of untreated dentin surface with exposed tubules

SEM of dentin surface showing occlusion of dentin tubules after application of Colgate Sensitive Pro-Relief TM Desensitizing Paste

In clinical trials, this product has been found to provide immediate and lasting relief of hypersensitivity for four weeks when it is applied in patients immediately after dental scaling, as the final polishing step during a professional cleaning procedure.57 A second study demonstrated its effectiveness in relieving dentinal hypersensitivity when applied prior to dental prophylaxis, with a significant reduction in dentinal hypersensitivity demonstrated postprocedurally.65 Based
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In-office paint-on surface treatments are a popular approach to treating root hypersensitivity, and are especially effective for localized dentinal hypersensitivity (single teeth). These products generally occlude and seal the dentin tubules. A variety of products has been reported to effectively reduce dentinal hypersensitivity, including resin-based materials.68-71 5% sodium fluoride varnish (Duraphat, Colgate-Palmolive, New York, NY) painted over exposed root surfaces has been shown to be an effective treatment for dentinal hypersensitivity.62 An aqueous solution of glutaraldehyde and hydroxyethylmethacrylate (HEMA) (Gluma Desensitizer, Heraeus-Kulzer; Calm-It, Dentsply-Caulk) has been reported to be an effective desensitizing agent for up to nine months.71,72 The mechanism for tubule occlusion appears to be due to the glutaraldehyde.73 The use of oxalates has also been shown to be effective, with the oxalate precipitating and occluding the open dentinal tubules.74 In addition, while there have not been any controlled studies on its effectiveness, anecdotal evidence suggests that burnishing a 0.5% solution of prednisolone onto exposed sensitive root surfaces may mitigate intractable hypersensitivity. Other treatment options include gingival grafts, adhesive resins, lasers and topically applied agents. Gingival grafts should be considered, in particular when the recession is progressive, there are aesthetic concerns or the sensitivity is unresponsive to more conservative treatment.75 When the exposed sensitive root surface has surface loss due to
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abrasion, erosion and/or abfraction leaving a notching of the root, consideration should be given to placing either an adhesive composite resin or glass ionomer restoration,76 which would both restore the tooth to full contour and seal the dentinal tubules. Lasers have been used successfully to seal open dentinal tubules either alone or with surface treatments.77-79 Iontophoresis can also be used, a technique that utilizes a low galvanic current to accelerate ionic exchanges and precipitation of insoluble calcium with fluoride gels to occlude the open tubules.80 Figure 9. In-office paint-on surface treatments

Recommendations for use and technique are product specific. The clinician needs to understand the in-office desensitizing agents to select one that is appropriate for the patient.

Professionally dispensed self-applied treatments

A professionally prescribed at-home treatment has been introduced (SootheRxTM, 3M/ESPE Preventive Care) that contains a calcium sodium phosphosilicate bioactive glass (NovaMin). This has been shown in vitro to seal and clog open dentinal tubules and to be effective for sensitivity relief after 6 weeks of home use.81,82 Amorphous calcium phosphate and casein phosphopeptide-amorphous calcium phosphate products (Relief ACP, Discus Dental; MI Paste, GC America) can also be used for desensitization by brushing them on the teeth, including before and after mouthguard or in-office bleaching. ACP has also been found to be effective for control of bleaching sensitivity when incorporated into bleaching gels.83-85 The use of ProClude, the precursor to Colgate Sensitive Pro-Relief Desensitizing Paste, was also reported to decrease sensitivity when used before bleaching.86 Self-applied over-the-counter treatments Over-the-counter (OTC) treatments for sensitive teeth can be the most cost-effective means to relieve sensitivity, and many people make the decision to self-medicate with desensitizing toothpastes. The claim of desensitizing teeth
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is a therapeutic claim and the toothpaste must contain an active ingredient that is recognized by the FDA as being an effective desensitizer at that concentration. For anything not recognized by the FDA as a desensitizing ingredient, a new drug application is required. The most popular desensitizing ingredient in toothpastes is potassium nitrate. According to the FDA monograph, for a potassium nitrate toothpaste to claim to be desensitizing, it must contain 5% potassium nitrate87 (Sensodyne, GlaxoSmithKline; Colgate Sensitive and Colgate Sensitive Enamel Protect, ColgatePalmolive; Crest Sensitivity, Procter & Gamble).The mode of action involves penetration of the potassium ions through the tubules to the A-fibers of the nerves, decreasing the excitability of these nerves.88-90 Many clinical trials have provided evidence of a reduction in tooth sensitivity with toothpastes containing potassium nitrate.91-94 These toothpastes may take up to two weeks to show any effectiveness. For best results, the toothpaste should be used twice a day as part of the persons oral care regimen. In recent years, vital bleaching has become very popular, with transient tooth sensitivity as a primary reported side effect with an incidence of 7% to 75%.95-99 For many patients, this is a barrier to continuing treatment, and 5% potassium nitrate desensitizing toothpaste has been recommended for patients undergoing bleaching.100,101 Two effective strategies using a 5% potassium nitrate desensitizing toothpaste are brushing with it for two weeks prior to initiating bleaching and having the patient place it into his or her bleaching tray and wear the tray for 30 minutes a day one week prior to the initiation of bleaching.100,101

Conclusion
As part of the routine dental examination and during every recall appointment, dental professionals should include in their patient questions queries about whether there are any sensitive teeth. Patients with dentinal hypersensitivity should be evaluated based upon risk factors and a proper diagnosis made, after which a treatment plan can be outlined for the patient. In most circumstances, the least invasive, most cost-effective treatment is the use of an effective desensitizing toothpaste. Depending on the severity of dentinal hypersensitivity, clinical management may include both in-office and self-applied at-home therapies, including recent and novel technologies that have been introduced.

References
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distribution of dentine sensitivity in a population of 17-58-yearolds serving on an RAF base in the Midlands. J Oral Rehabil. 2002; 29:14-23. Al-Sabbagh M, Andreanna S, Ciancio SG. Dentinal hypersensitivity: review of aetiology, differential diagnosis, prevalence and mechanism. J Int Acad Periodontol. 2004; 6(1):8-12. Fischer C, Fischer RG, Wennberg A. Prevalence and distribution of cervical dentine hypersensitivity in a population in Rio de Janeiro. Brazil J Dent. 1992; 20:272-76. Liu HC, Lan WH, Hsieh CC. Prevalence and distribution of cervical dentin hypersensitivity in a population in Taipei, Taiwan. J Endod. 1998; 24:45-7. Taani DQ, Awartani F. Prevalence and distribution of dentin hypersensitivity and plaque in a dental hospital population. Quintessence Int. 2001; 32:372-6. Rees JS, Addy M. A cross-sectional study of dentine hypersensitivity. J Clin Periodontol. 2002; 29:997-1003. Chabanski MB, Gillam DG, Bulman JS, et al. Prevalence of cervical dentine sensitivity in a population of patients referred to a specialist periodontology department. J Clin Periodontol. 1996; 23:989-92. von Troil B, Needleman E, Sanz M. A systematic review of the prevalence of root sensitivity following periodontal therapy. J Clin Periodontol. 2002; 29(Suppl) 3:173-7. Addy M. Dentine hypersensitivity: Definition, prevalence, distribution and aetiology. In Addy M, Embery G, Edgar WM, Orchardson R, eds. Tooth wear and sensitivity: Clinical advances in restorative dentistry. London, Martin Dunitz; 2000:239-48. Addy M. Dentine hypersensitivity: New perspectives on an old problem. Int Dent J. 2002; 52:375-6. Orchardson R, Collins WJ. Clinical features of hypersensitive teeth. Br Dent J. 1987; 162:253-6. Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity: The distribution of recession, sensitivity and plaque. J Dent. 1987; 15:242-8. Gillam DG, Seo HS, Bulman JS, Newman HN. Perceptions of dentine hypersensitivity in a general practice population. J Oral Rehabil. 1999; 26:710-4. Strassler HE, Gerhardt DE. Troubleshooting everyday restorative emergencies. Dent Clin North Am. 1993; 37(3):353-65. Panagakos F, Schiff T, Guignon A. Dentin hypersensitivity: Effective treatment with an in-office desensitizing paste containing 8% arginine and calcium carbonate. Am J Dent. 2009; 22(Special Issue): 3A-7A. Strassler HE, Serio F. Managing dentin hypersensitivity. Inside Dentistry 2008; 4(7):73-8. Curro FA. Tooth hypersensitivity in spectrum of pain. Dent Clin North Am. 1990; 34:429-37. Calvo P. Treatment of sensitive dentine. Dent Cosmos. 1884;13941. Orchardson R, Gillam GC. Managing dentin hypersensitivity. J Am Dent Assoc. 2006; 137:990-8. Pashley DH, Tay FR, Haywood VB, Collins MC, Drisko CL. Dentin hypersensitivity: Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. Inside Dentistry. 2008; 4(Special Issue): I-35. Canadian Advisory Board on Dentin Hypersensitivity. Consensusbased recommendations for the diagnosis and management of dentin hypersensitivity. J Can Dent Assoc. 2003; 69:221-6. Idle M. The differential diagnosis of sensitive teeth. Dent Update. 1998; 25:462-6. Ailor JE Jr. Managing incomplete tooth fractures. J Am Dent Assoc. 2000; 131:1158-74. Johnson DC. Innervation of the dentin, predentin and pulp. J Dent Res. 1985; 64(Special Issue):555-63. Brnnstrm M. Dentin sensitivity and aspiration of odontoblasts. J Am Dent Assoc. 1963; 66:366-70. Cummins D. Dentin hypersensitivity: From diagnosis to a breakthrough therapy for everyday sensitivity relief. J Clin Dent. 2009; 20(Special Issue):1-9. Absi EG, Addy M, Adams D. Dentine hypersensitivity: A study of the patency of dentinal tubules in sensitive and non-sensitive cervical dentine. J Clin Periodontol. 1987; 14(5):280-4. Kim S. Hypersensitive teeth: Desensitization of pulpal nerves. J Endod. 1986; 12:482-5. Jacobsen PL, Bruce G. Clinical dental hypersensitivity: Understanding the causes and prescribing a treatment. J Contemp Dent Pract. 2001; 2(1):1-8.

34 Beltran-Aguilar ED, Barker LK, Canto MT, Dye BA, et al. Centers for Disease Control and Prevention (CDC). Surveillance for dental caries, dental sealants, tooth retention, edentulism and enamel fluorosis United States, 1988-1994 and 1999-2002. MMWR Surveill Summ 2005; 54(3):1-43. 35 Holland GR, Narhi MN, Addy M, et al. Gingival recession, gingival bleeding and dental calculus in adults 30 years of age and older in the United States, 1988-1994. J Periodontol. 1999; 70:30-43. 36 Tugnait A, Clerehugh V. Gingival recession its significance and management. J Dent. 2001; 29:381-94. 37 Canakci CF, Canakci V. Pain experienced by patients undergoing different periodontal therapies. J Am Dent Assoc. 2007; 138:156373. 38 Kumar PS, Leblebicioglu B. Pain control during nonsurgical periodontal therapy. Compend Contin Educ Dent. 2007; 28:666-70. 39 Piotrowski BT, Gillette WB, Hancock EB. Examining the prevalence and characteristics of abfractionlike cervical lesions in a population of U.S. veterans. J Am Dent Assoc. 2001; 132:1694-701. 40 Braem M, Lambrechts P, Vanderle G. Stress induced cervical lesions. J Prosthet Dent. 1992; 67:718-22. 41 Smith GBN, Knight JK. A comparison of patterns of tooth wear with the etiologic factors. Br Dent J. 1984; 157:16-19. 42 Grippo JO. Abfraction: A new classification of hard tissue lesions of teeth. J Esthet Dent. 1991; 3:14-19. 43 Eik JD, Wilko RA, Anderson CH, Sorensen SE. Scanning electron microscopy of cut tooth surfaces and identification of debris by use of electron microprobe. J Dent Res. 1970; 49:1359-68. 44 Pashley DH. Smear layer: biologic considerations. Oper Dent Suppl. 1984; 3:13-29. 45 Addy M. Tooth brushing, tooth wear and dentine sensitivity are they associated? Int Dent J. 2005; 55(4 Suppl 1):261-7. 46 Corra FOB, Sampaio JEC, Jnior CR, Orrico SRP. Influence of natural fruit juices in removing the smear layer from root surfaces an in vitro study. J Can Dent Assoc. 2004; 70:697-702. 47 Rees JS, Loyn T, Rowe W, Kunst Q, et al. The ability of fruit teas to remove the smear layer: An in vitro study of tubule patency. J Dent. 2005; 34:67-76. 48 Mongiorgi R, Sauro S, Bernardi F, et al. Dentinal hypersensitivity induced by acid drinks: An innovative phytocomplexes based treatment. J Dent Res. 2006;85(Spec Issue A):Abstract no. 2063. 49 Geurtsen W. Rapid general dental erosion by gas-chlorinated swimming pool water. Review of the literature and case report. Am J Dent. 2000; 13:291-3. 50 Carlaio RG, Grassi RF, Losacco T, et al. Gastroesophageal reflux disease and dental erosion: A case report and review of the literature. Clin Ter. 2007; 158:349-53. 51 Lussi A, Hellwig E. Risk assessment and preventive measures. Monogr Oral Sci. 2006;20:190-9. 52 Schuurs AH, Wesselink PR, Eijkman MA, Duivenvoorden HJ. Dentists views on cervical hypersensitivity and their knowledge of its treatment. Endod Dent Traumatol. 1995;11(5):240-4. 53 Gillam DG, Bulman JS, Eijkman MA, Newman HN. Dentists perceptions of dentine hypersensitivity and knowledge of its treatment. J Oral Rehabil. 2002; 29:219-25. 54 Gunsolley JC. The need for pain control during scaling and root planning. Compend Contin Educ Dent. 2005; 26(2 Suppl 1):3-5. 55 Friskopp J, Nilsson M, Isacsson G. The anesthetic onset and duration of a new lidocaine/prilocaine gel intra-pocket anesthetic (Oraqix) for periodontal scaling/root planing. J Clin Periodontol. 2001; 28:453-8. 56 Kleinberg I. Sensistat: A new saliva-based composition for simple and effective treatment of dentinal sensitivity pain. Dent Today. 2002; 21:42-7. 57 Schiff T, Delgado E, Zhang YP, et al. Clinical evaluation of the efficacy of an in-office desensitizing paste containing 8% arginine and calcium carbonate in providing instant and lasting relief of dentin hypersensitivity. Am J Dent. 2009; 22 (Spec Issue):8A-15A. 58 Orchardson R, Gangarosa LP, Holland GR, et al. Dentine hypersensitivity into the 21st century. Arch Oral Biol. 1994; 39 (Suppl):113S-9S. 59 Vieira AHM, Santiago SL. Management of dentinal hypersensitivity. Gen Dent. 2009; 57:120-6. 60 Sengupta K, Lawrence HP, Limeback H, et al. Comparison of power and manual toothbrushes in dentine sensitivity. J Dent Res. (Spec Issue A). 2005; 84: Abstr. 942. 61 Drisko CH. Dentine hypersensitivity - dental hygiene and periodontal considerations. Int Dent J. 2002;52:385-393

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62 Gaffar A. Treating hypersensitivity with fluoride varnishes. Compend Contin Educ Dent. 1988; 19:1088-97. 63 Al-Sabbagh M, Brown A, Thomas MV. In-office treatment of dentinal hypersensitivity. Dent Clin North Am. 2009; 53(1):47-60. 64 Wynn RL, Meiller TF, Crossley HL. Lexi-Comps Drug Information Handbook for Dentistry. Lexi-Comp, 2008. 65 Hamlin D, Phelan Williams E, Delgado E, et al. Clinical evaluation of the efficacy of a desensitizing paste containing 8% arginine and calcium carbonate for the in-office relief of dentin hypersensitivity associated with dental prophylaxis. Am J Dent. 2009; 22:16A-20A. 66 Garcia-Godoy F, Garcia-Godoy A, Garcia-Godoy C. Effect of a desensitizing paste containing 8% arginine and calcium carbonate on the surface roughness of dental materials and human enamel. Am J Dent. 2009; 22(Special Issue):21A-3A. 67 Petrou I, Heu R, Stranick M, et al. A breakthrough therapy for dentin hypersensitivity:dental products containing 8% arginine and calcium carbonate work to deliver effective relief of sensitive teeth. J Clin Dent. 2009;20(Spec Iss):23-31. 68 Duran I, Sengun A. The long-term effectiveness of five current desensitizing products on cervical dentine sensitivity. J Oral Rehabil. 2004; 31:351-6. 69 Dondi dallOrologio G, Lorenzi R, et al. Dentin desensitizing effects of Gluma Alternative, Health-Dent Desensitizer, and Scotchbond Multi-Purpose. Am J Dent. 1999; 12:103-6. 70 Pamir T, Dalgar H, Onal B. Clinical evaluation of three desensitizing agents in relieving dentin sensitivity. Oper Dent. 2007; 32:544-8. 71 Kakaboura A, Rahiotis C, Thomaidis S, Doukoudakis S. Clinical effectiveness of two agents on the treatment of tooth cervical hypersensitivity. Am J Dent. 2005; 18:291-5. 72 Schpback P, Lutz F, Finger WJ. Closing of dentinal tubules by Gluma desensitizer. Eur J Oral Sci. 1997; 105:414-21. 73 Yiu CK, Hiraishi N, Chersoni S, Breschi L, et al. Single bottle adhesives behave as permeable membranes after polymerisation. II. Differential permeability reduction with an oxalate desensitiser. J Dent. 2006; 34:106-16. 74 Crispin BJ. Dentin sensitivity and the clinical evaluation of a unique dual-action dentin desensitizer. Contemp Esthet Restor Pract. 2001; 8(3)(Suppl):3-7. 75 Fombellida Cortazar F, Sanz Dominguez JR, et al. A novel surgical approach to marginal soft tissue recessions: Two-year results of 11 case studies. Pract Proceed Aesthet Dent. 2002; 14:749-54. 76 Starr GB. Class 5 restorations. In Summitt JB, Robbins JW, Schwartz RS, eds. Fundamentals of Operative Dentistry: A Contemporary Approach. 2nd edition. Quintessence Books, Chicago. p. 386-400. 77 Schwarz F, Arweiler N, Georg T, Reich E. Desensitizing effects of an Er:YAG laser on hypersensitive dentine. J Clin Periodontol. 2002; 29:211-5. 78 Gelskey SC, White JM, Pruthi VK. The effectiveness of the Nd:YAG laser in the treatment of dentin hypersensitivity. J Can Dent Assoc. 1993; 59:377-86. 79 Lee B, Chang C, Chen W, Lan W, et al. In vitro study of dentin hypersensitivity treated by Nd:YAP laser and bioglass. Dent Mater. 2005;21(6):511-9. 80 Gangarosa L Sr. Iontophoretic application of fluoride in tray techniques for desensitizing multiple teeth. J Am Dent Assoc. 1981; 95:50-2. 81 Gillam DG, Tang JY, Mordan NJ, Newman HN. The effects of a novel bioglass dentifrice on dentine sensitivity: A scanning electron microscopy investigation. J Oral Rehabil. 2002; 29:305-13. 82 Du MQ, Tai BJ, Jiang H, et al. Efficacy of dentifrice containing bioactive glass (NovaMin) on dentine hypersensitivity. J Dent Res. 2004; 83(Special Issue A):Abstract 1546. 83 Giniger M, Macdonald J, Siemba S, et al. The clinical performance of professionally dispensed bleaching gel with added amorphous calcium phosphate. J Am Dent Assoc. 2005; 136:383-92. 84 Matis B, Cochran MA, Ekert GJ, Matis JL. In vivo study of two carbamide peroxide gels with different desensitizing agents. Oper Dent. 2007; 32:549-55. 85 Geiger S, Matalon S, Blashalg J, et al. The clinical effect of amorphous calcium phosphate (ACP) on root surface sensitivity. Oper Dent. 2003; 28:496-500. 86 Rosen B. A successful approach to whitening without dentinal sensitivity. Dent Today. 2005; 24(12):62-4. 87 Federal Register, Vol. 57 No. 91, May 11, 1992; 20114-5. 88 Markowitz K, Bilotto G, Kim S. Decreasing intradental nerve activity in the cat with potassium and divalent cations. Archives of Oral Biol. 1991; 36:1-7.

89 Peacock JM, Orchardson R. Effects of potassium ions on action potential conduction in A- and C-fibers of rat spinal nerves. J Dent Res. 1995; 74:634-41. 90 Markowitz K, Kim S. The role of selected cations in the desensitization of intradental nerves. Proc Finn Dent Soc. 1992; 88(Suppl) 1:39-54. 91 Sowinski J, Avad F, Petrone M, et al. Comparative investigations of the desensitizing efficacy of a new dentifrice. J Clin Periodontol. 2001; 28:1032-6. 92 Avad F, Berta R, DeVizio W, et al. Comparative efficacy of two dentifrices containing 5% potassium nitrate on dentinal sensitivity: A twelve-week clinical study. J Clin Dent. 1994; 5 (Spec):97-101. 93 Conforti N, Battista GW, Petrone DM, et al. Comparative investigation of the desensitizing efficacy of a new dentrifice: A 14-day clinical trial. Compend Contin Educ Dent. 2000; 27(Suppl):17-22. 94 Schiff T, Zhang YP, DeVizio W, et al. A randomized clinical trial of the desensitizing efficacy of three dentifrices. Compend Contin Educ Dent. 2000; 27(Suppl):4-10. 95 Haywood VB. Treating sensitivity during tooth whitening. Compend Contin Educ Dent. 2005; 26(Suppl):11-20. 96 Haywood VB, Leonard RH, Nelson CF, et al. Effectiveness, side effects and long-term status of nightguard vital bleaching. J Am Dent Assoc. 1994; 125:1219-26. 97 Swift EJ, May KN, Wilder AD, et al. Six-month clinical evaluation of a tooth whitening systems using an innovative experimental design. J Esthet Dent. 1997; 9:265-74. 98 Matis BA, Cochran MA, et al. The efficacy and safety of a 10% carbamide peroxide bleaching gel. Quintess Int. 1994; 29:555-63. 99 Leonard RH, Bentley C, Eagle JC, et al. Nightguard vital bleaching: A long-term study on efficacy, shade retention, side effects, and patients perceptions. J Esthet Restor Dent. 2001;13:357-69. 100 Haywood VB, Cordero R, Wright K, et al. Brushing with a potassium nitrate dentifrice to reduce bleaching sensitivity. J Clin Dent. 2005; 16:17-22. 101 Leonard RH Jr., Smith LR, Garland GE, Caplan DJ. Desensitizing agent efficacy during whitening in an at-risk population. J Esthet Restor Dent. 2004; 16:49-55.

Author Profile

Dr. Howard Strassler is professor and director of operative dentistry at the University of Maryland Dental School in the Departments of Endodontics, Prosthodontics, and Operative Dentistry. He is a fellow in the Academy of Dental Materials and the Academy of General Dentistry, a member of the American Dental Association, the Academy of Operative Dentistry, and the International Association for Dental Research. Dr. Strassler has published more than 400 articles in the field of restorative dentistry and innovations in dental practice, coauthored seven chapters in texts, and lectured nationally and internationally. Dr. Strassler has a general practice in Baltimore, Maryland, limited to restorative dentistry and aesthetics. Dr. Francis Serio is professor and chairman of the department of periodontics and preventive sciences at the University of Mississippi School of Dentistry, and a Diplomate of the American Board of Periodontology. Dr. Serio completed his undergraduate studies at The Johns Hopkins University and received his DMD from the University of Pennsylvania. He earned his MS and certificate in Periodontics at the University of Maryland and his MBA from Millsaps College. Dr. Serio has presented over 120 lectures and continuing education courses in the U.S. and internationally, and has written or coauthored over 35 scientific articles and four books. Disclaimer The authors of this course have no commercial ties with the sponsor or provider of the unrestricted educational grant for this course. Reader Feedback We encourage your comments on this or any PennWell course. For your convenience, an online feedback form is available at www. ineedce.com.
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Online Completion
Use this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the Online Courses listing and complete the online purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the Take Exam link, complete all the program questions and submit your answers. An immediate grade report will be provided and upon receiving a passing grade your Verification Form will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime in the future by returning to the site, sign in and return to your Archives Page.

Questions
1. Dentinal hypersensitivity has been referred to as one of the most painful and least successfully treated chronic dental conditions.
a. True b. False

12. Biofilm deposits on root surfaces may increase hypersensitivity.

a. True b. False

2. The prevalence of dentinal hypersensitivity has been reported to be between ____________ in the general population, and among periodontal patients, its frequency is considerably higher ___________.
a. b. c. d. 4% and 37%; 40%68% 4% and 57%; 40%68% 4% and 37%; 60%98% 4% and 57%; 60%98%

13. One survey of dentists and dental hygienists found that fewer than half of respondents considered a differential diagnosis for dentinal hypersensitivity, even though it is by definition a diagnosis of exclusion.
a. True b. False

c. binding to the negatively charged dentin surface and helping to attract a calcium-rich layer from the saliva to infiltrate and block the dentin tubules d. none of the above

22. In-office paint-on surface treatments are a popular approach to treating root hypersensitivity.
a. True b. False

14. Patients with unresolved hypersensitivity over many years provide the dental professional with varied ___________ clues.
a. b. c. d. behavioral and censorial postural and censorial postural and behavioral none of the above

23. An aqueous solution of glutaraldehyde and HEMA has been reported to be an effective desensitizing agent for up to ___________.
a. b. c. d. three months six months nine months one year

3. The canines and molars are reported to be affected most often by dentinal hypersensitivity.
a. True b. False

4. Patients may experience dentinal hypersensitivity ___________.

a. episodically in response to stimuli b. during routine and normal actions associated with dental treatment c. postoperatively after dental treatment such as scaling and root planing d. all of the above

15. As part of any screening for dentinal hypersensitivity, the clinician should assess whether there is a localized or generalized problem.
a. True b. False

24. Several controlled studies have demonstrated the effectiveness of burnishing a 0.5% solution of prednisolone onto exposed sensitive root surfaces to mitigate intractable hypersensitivity.
a. True b. False

5. Conditions that need to be ruled out before making a diagnosis of dentinal hypersensitivity include but are not limited to ___________.
a. b. c. d.

16. If a tooth or teeth are predisposed to dentin hypersensitivity, they can be definitively treated once and for all and with no need for the problem to be a future consideration.
a. True b. False

occlusal trauma caries and fractured or cracked teeth potential reversible or irreversible pulpal pathology all of the above

25. When the exposed sensitive root surface has surface loss due to abrasion, erosion and/or abfraction leaving a notching of the root, consideration should be given to placing ___________.
a. a temporary restoration b. an adhesive composite resin or a glass ionomer restoration c. a luting cement or a liner d. none of the above

17. Avoiding brushing teeth immediately after the ingestion of acidic foods is a ___________ for dentinal hypersensitivity.
a. treatment recommendation b. preventive recommendation c. requirement only if the patient uses a hard-bristled brush d. problem

6. For human dentin, one square millimeter of dentin can contain 30,000 tubules, depending on depth.
a. True b. False a. b. c. d.

7. The most widely accepted mechanism of dentin sensitivity is the ___________.

hydrostatic theory pulpal sensory nerve activity theory hydrodynamic theory none of the above

18. The two major groups of products used to treat dentin hypersensitivity are

26. The clinician needs to understand the in-office desensitizing agents to select one that is appropriate for the patient.
a. True b. False

8. Exposed root surfaces due to gingival recession are ___________ predisposing factor to dentinal root hypersensitivity.
a. b. c. d. a minor a major the only none of the above

a. those that remove dentinal tubules, and those that enhance transmission of neural impulses b. those that occlude and block dentinal tubules, and those that enhance transmission of neural impulses c. those that occlude and block dentinal tubules, and those that interfere with the transmission of neural impulses d. none of the above

27. Calcium sodium phosphosilicate bioactive glass, as well as amorphous calcium phosphate, has been found to be effective in treating dentinal hypersensitivity.
a. True b. False

9. Fear of pain and discomfort during subgingival instrumentation has been reported to deter ___________ of the population from seeking treatment.
a. b. c. d. 5% 10% 15% 20%

19. When treating patients with an in-office professional treatment, the American Dental Association treatment codes that can be noted for insurance reimbursement are ___________.
a. b. c. d. D9910 and D9920 D8810 and D9910 D9910 and D9911 none of the above

28. According to an FDA monograph, for a potassium nitrate toothpaste to claim to be desensitizing, it must contain ___________.
a. b. c. d. 3% potassium nitrate 5% potassium nitrate 7% potassium nitrate 10% potassium nitrate

10. Enamel loss with exposed dentin due to attrition and tooth wear due to bruxism, occlusal habits and other forms of parafunctional activity can contribute to the etiology of dentinal hypersensitivity.
a. True b. False a. b. c. d.

20. Eight percent arginine and calcium carbonate paste has been shown to occlude the dentin tubules and to provide significant relief for patients postoperatively after scaling and root planing and oral prophylaxis.
a. True b. False

29. Using 5% potassium nitrate desensitizing toothpaste and brushing with it for two weeks prior to initiating bleaching is effective in reducing dentinal hypersensitivity associated with bleaching.
a. True b. False

11. Loss of the ___________ contributes to dentinal hypersensitivity.

intaglia smear layer myelinated and nonmyelinated nerve fibers all of the above

21. Arginine provides relief from hypersensitivity by ___________.

a. binding to the negatively charged oral mucosa and helping to attract a fluoride-rich layer to infiltrate and block the dentin tubules b. binding to the positively charged dentin surface and helping to attract a calcium-rich layer from the saliva to infiltrate and block the dentin tubules

30. Depending on the severity of the condition, clinical management of dentinal hypersensitivity may include both in-office and self-applied at-home therapies.
a. True b. False

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ANSWER SHEET

Dentinal Hypersensitivity: Etiology, Diagnosis and Management

Name: Address: City: Telephone: Home ( ) Title: E-mail: State: Office ( ) ZIP: Country: Specialty:

Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 4 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp.

Educational Objectives
1. Know the incidence of dentinal hypersensitivity and risk factors for this condition 2. Know the anatomical and physiological features, and the accepted theory, associated with dentinal hypersensitivity 3. Understand the need for screening and diagnosis by exclusion for dentinal hypersensitivity 4. Know the treatment options available for dentinal hypersensitivity and considerations in selecting these

If not taking online, mail completed answer sheet to

Academy of Dental Therapeutics and Stomatology,

A Division of PennWell Corp.

P.O. Box 116, Chesterland, OH 44026 or fax to: (440) 845-3447

For immediate results, go to www.ineedce.com to take tests online. answer sheets can be faxed with credit card payment to (440) 845-3447, (216) 398-7922, or (216) 255-6619. P  ayment of $59.00 is enclosed. (Checks and credit cards are accepted.) If paying by credit card, please complete the following: MC Visa AmEx Discover Acct. Number: _______________________________

Course Evaluation
Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0. 1. Were the individual course objectives met? Objective #1: Yes No Objective #2: Yes No 2. To what extent were the course objectives accomplished overall? 3. Please rate your personal mastery of the course objectives. 4. How would you rate the objectives and educational methods? 5. How do you rate the authors grasp of the topic? 6. Please rate the instructors effectiveness. 7. Was the overall administration of the course effective? 8. Do you feel that the references were adequate? 9. Would you participate in a similar program on a different topic? 5 5 5 5 5 5 4 4 4 4 4 4 Yes Yes Objective #3: Yes No Objective #4: Yes No 3 3 3 3 3 3 2 2 2 2 2 2 No No 1 1 1 1 1 1 0 0 0 0 0 0

Exp. Date: _____________________ Charges on your statement will show up as PennWell

10. If any of the continuing education questions were unclear or ambiguous, please list them. ___________________________________________________________________ 11. Was there any subject matter you found confusing? Please describe. ___________________________________________________________________ ___________________________________________________________________ 12. What additional continuing dental education topics would you like to see? ___________________________________________________________________ ___________________________________________________________________ PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.
AUTHOR DISCLAIMER The authors of this course have no commercial ties with the sponsor or the provider of the unrestricted educational grant for this course. SPONSOR/PROVIDER This course was made possible through an unrestricted educational grant from Colgate-Palmolive Company. No manufacturer or third party has had any input into the development of course content. All content has been derived from references listed, and or the opinions of clinicians. Please direct all questions pertaining to PennWell or the administration of this course to Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or macheleg@pennwell.com. COURSE EVALUATION and PARTICIPANT FEEDBACK We encourage participant feedback pertaining to all courses. Please be sure to complete the survey included with the course. Please e-mail all questions to: macheleg@pennwell.com. INSTRUCTIONS All questions should have only one answer. Grading of this examination is done manually. Participants will receive confirmation of passing by receipt of a verification form. Verification forms will be mailed within two weeks after taking an examination. EDUCATIONAL DISCLAIMER The opinions of efficacy or perceived value of any products or companies mentioned in this course and expressed herein are those of the author(s) of the course and do not necessarily reflect those of PennWell. Completing a single continuing education course does not provide enough information to give the participant the feeling that s/he is an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise. COURSE CREDITS/COST All participants scoring at least 70% (answering 21 or more questions correctly) on the examination will receive a verification form verifying 4 CE credits. The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership credit. Please contact PennWell for current term of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. PennWell is a California Provider. The California Provider number is 4527. The cost for courses ranges from $49.00 to $110.00. Many PennWell self-study courses have been approved by the Dental Assisting National Board, Inc. (DANB) and can be used by dental assistants who are DANB Certified to meet DANBs annual continuing education requirements. To find out if this course or any other PennWell course has been approved by DANB, please contact DANBs Recertification Department at 1-800-FOR-DANB, ext. 445. RECORD KEEPING PennWell maintains records of your successful completion of any exam. Please contact our offices for a copy of your continuing education credits report. This report, which will list all credits earned to date, will be generated and mailed to you within five business days of receipt. CANCELLATION/REFUND POLICY Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing. 2009 by the Academy of Dental Therapeutics and Stomatology, a division of PennWell

AGD Code 010

DENT119RDH

SO407305
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